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Publication Insights

  • A research team from China Medical University published a study in Advanced Science, elucidating the critical role of protein arginine deiminase family member PAD1 in maintaining ovarian cancer stem cell (OCSLC) characteristics and drug resistance. The study found that PAD1 is significantly upregulated in ovarian cancer tissues, correlating with malignant phenotypes and stemness. PAD1 specifically interacts with AKT2, catalyzing its citrullination at the R202 site, thereby activating the PI3K/AKT signaling pathway and upregulating the transcription factor CEBPβ to promote the expression of stemness marker genes. Inhibiting PAD1 reduces AKT2 phosphorylation and citrullination, reversing stemness features and cisplatin resistance, with synergistic effects when combined with AKT inhibitors. The site-specific AKT2-Cit202 monoclonal antibody provided by AtaGenix played a pivotal role in validating this mechanism, offering new insights into potential therapeutic targets for ovarian cancer.
  • A study from Tongji Medical College, published in Cancer Research, explores the role of RNA splicing abnormalities in tumor metabolic reprogramming, focusing on the SLK gene’s exon 13 skipping variant, SLKv. The research demonstrates that SLKv enhances glycolysis by directly phosphorylating Enolase 1 (ENO1) at Ser2, increasing its activity and driving phosphoenolpyruvate (PEP) accumulation. This forms a positive feedback loop activating key glycolytic enzymes, promoting tumor growth. The TGFβ-KHDRBS1 signaling axis was identified as an upstream regulator of SLKv splicing. Antisense oligonucleotides (ASOs) targeting SLKv reduced glycolysis and tumor growth, highlighting a potential therapeutic strategy. This study reveals a novel mechanism linking RNA splicing to metabolic reprogramming in cancer.
  • Perioperative Neurocognitive Disorders (PND) affect up to 40% of elderly surgical patients, leading to prolonged hospitalization and increased care costs without FDA-approved treatments. This study explores the C3/C3aR complement pathway’s role in driving neuroinflammation and the potential of platelet factor 4 (PF4) as a protective factor. Using AtaGenix’s custom-synthesized CR2-crry inhibitor, researchers demonstrated in clinical and animal models that targeting C3 reduces inflammation and cognitive decline, while PF4 supplementation enhances cognitive recovery and neuronal repair. These findings highlight novel therapeutic targets for PND, with CR2-crry showing promising clinical translation potential.
  • Using the custom insect-cell–expressed SERBP1 recombinant protein provided by Atagenix, researchers uncovered the pivotal role of the PCIF1–SERBP1 complex in modulating neuronal function under nerve injury conditions. The study revealed that the complex promotes m⁶Am modification of Maf1 mRNA, resulting in reduced MAF1 protein levels and heightened neuronal excitability, thereby
  • A research team from Westlake Laboratory of Life Sciences and Biomedicine published a study in Immunity, elucidating the molecular mechanisms by which meningeal B cells drive neuroinflammatory relapse in multiple sclerosis (MS) through antigen presentation and cognate interactions with T cells. Using the experimental autoimmune encephalomyelitis (EAE) model, combined with single-cell RNA sequencing and immunofluorescence, the study revealed that meningeal autoreactive B cells, activated by MOG antigens, promote T cell-mediated inflammation via MHC-II-mediated antigen presentation, forming a “T-B cell-neutrophil-endothelial cell” inflammatory loop. Targeted depletion of local brain B cells effectively alleviated EAE relapse, offering new directions for MS precision therapy. AtaGenix provided high-purity MOG protein, supporting key experimental validations.
  • Alzheimer's disease (AD) is the most common form of dementia, causing significant social and economic impact. Its characteristic neuropathological features include β-amyloid (Aβ) deposition, tau hyperphosphorylation, and the loss of synapses and neurons. In recent years, studies have shown that chronic inflammation mediated by local and peripheral immune cells also plays a critical role in the pathogenesis of AD.
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